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Author: Lawrence Rosenthal, MD, PhD, FACC, FHRS; Chief Editor: Jeffrey N
Rottman, MD more...
Atrial flutter is a cardiac arrhythmia characterized by atrial rates of 240-400 beats/min and
some degree of atrioventricular (AV) node conduction block. For the most part, morbidity
and mortality are due to complications of rate (eg, syncope and congestive heart failure
[CHF]). See the image below.
Signs and symptoms in patients with atrial flutter typically reflect decreased cardiac output as
a result of the rapid ventricular rate. Typical symptoms include the following:
Palpitations
Mild dyspnea
Presyncope
Less common symptoms include angina, profound dyspnea, or syncope. Tachycardia may or
may not be present, depending on the degree of AV block associated with the atrial flutter
activity.
Physical findings include the following:
If embolization has occurred from intermittent atrial flutter, findings are related to brain or
peripheral vascular involvement. Other complications of atrial flutter may include the
following:
CHF
Severe bradycardia
Transthoracic echocardiography (TTE) is the preferred modality for evaluating atrial flutter.
It can evaluate right and left atrial size, as well as the size and function of the right and left
ventricles, and this information facilitates diagnosis of valvular heart disease, left ventricular
hypertrophy (LVH), and pericardial disease.
See Workup for more detail.
Management
General treatment goals for symptomatic atrial flutter are similar to those for atrial
fibrillation. They include the following:
Control of ventricular rate This can be achieved with drugs that block the
AV node; intravenous (IV) calcium channel blockers (eg, verapamil and
diltiazem) or beta blockers can be used, followed by initiation of oral
agents
Background
Atrial flutter is a cardiac arrhythmia characterized by atrial rates of 240-400 beats/min,
usually with some degree of atrioventricular (AV) node conduction block. In the most
common form of atrial flutter (type I atrial flutter), electrocardiography (ECG) demonstrates
a negative sawtooth pattern in leads II, III, and aVF.
Type I (typical or classic) atrial flutter involves a single reentrant circuit with circus
activation in the right atrium around the tricuspid valve annulus. The circuit most often
travels in a counterclockwise direction. Type II (atypical) atrial flutter follows a different
circuit; it may involve the right or the left atrium. (See Pathophysiology.)
Atrial flutter is associated with a variety of cardiac disorders. In most studies, approximately
60% of patients with atrial flutter have coronary artery disease (CAD) or hypertensive heart
disease; 30% have no underlying cardiac disease. Uncommon forms of atrial flutter have
been noted during long-term follow-up in as many as 26% of patients with surgical correction
of congenital cardiac anomalies. (See Etiology.)
Symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result
of the rapid ventricular rate. The most common symptom is palpitations. Other symptoms
include fatigue, dyspnea, and chest pain. (See Presentation.) ECG is essential in making the
diagnosis. Transthoracic echocardiography (TTE) is the preferred modality for evaluating
atrial flutter. (See Workup.)
Intervening to control the ventricular response rate or to return the patient to sinus rhythm is
important. Consider immediate electrical cardioversion for patients who are
hemodynamically unstable. Consider catheter-based ablation as first-line therapy in patients
with type I typical atrial flutter if they are reasonable candidates. Ablation is usually done as
an elective procedure; however, it can also be done when the patient is in atrial flutter. (See
Treatment.)
Atrial flutter is similar to atrial fibrillation in many respects (eg, underlying disease,
predisposing factors, complications, and medical management), and some patients have both
atrial flutter and atrial fibrillation. However, the underlying mechanism of atrial flutter makes
this arrhythmia amenable to cure with percutaneous catheter-based techniques.
Pathophysiology
In humans, the most common form of atrial flutter (type I) involves a single reentrant circuit
with circus activation in the right atrium around the tricuspid valve annulus (most often in a
counterclockwise direction), with an area of slow conduction located between the tricuspid
valve annulus and the coronary sinus ostium (subeustachian isthmus). A 3-dimensional
electroanatomic map of type I atrial flutter is shown in the video below.
3-Dimensional electroanatomic map of type I atrial flutter. Colors progress from
blue to red to white and represent relative conduction time in right atrium (early
to late). Ablation line (red dots) has been created on tricuspid ridge extending to
inferior vena cava. This interrupts flutter circuit. RAA = right atrial appendage;
CSO = coronary sinus os; IVC = inferior vena cava; TV = tricuspid valve annulus.
Animal models have been used to demonstrate that an anatomic block (surgically created) or
a functional block of conduction between the superior vena cava and the inferior vena cava,
similar to the crista terminalis in the human right atrium, is key to initiating and maintaining
the arrhythmia.
The crista terminalis acts as another anatomic conduction barrier, similar to the line of
conduction block between the 2 venae cavae required in the animal model. The orifices of
both venae cavae, the eustachian ridge, the coronary sinus orifice, and the tricuspid annulus
complete the barrier for the reentry circuit (see the image below). Type I atrial flutter is often
referred to as isthmus-dependent flutter. Usually, the rhythm is due to reentry, there is an
excitable gap, and the rhythm can be entrained.
Type I counterclockwise atrial flutter. This 3dimensional electroanatomic map of tricuspid valve and right atrium shows
activation pattern displayed in color format. Red is early and blue is late, relative
to fixed point in time. Activation travels in counterclockwise direction.
Type I atrial flutter can also have the opposite activation sequence (ie, clockwise activation
around the tricuspid valve annulus). Clockwise atrial flutter is much less common. When the
electric activity moves in a clockwise direction, the ECG will show positive flutter waves in
leads II, III, and aVF and may appear somewhat sinusoidal. This arrhythmia is still
considered type I, isthmus-dependent flutter; it is usually called reverse typical atrial flutter.
Type II (atypical) atrial flutters are less extensively studied and electroanatomically
characterized. Atypical atrial flutters may originate from the right atrium, as a result of
surgical scars (ie, incisional reentry), or from the left atrium, specifically the pulmonary veins
(ie, focal reentry) or mitral annulus (see the image below). Left atrial flutter is common after
incomplete left atrial linear ablation procedures (for atrial fibrillation). Thus, tricuspid
isthmus dependency is not a prerequisite for type II atrial flutter.
Etiology
Atrial flutter is associated with a variety of cardiac disorders. In most studies, approximately
30% of patients with atrial flutter have CAD, 30% have hypertensive heart disease, and 30%
have no underlying cardiac disease. Rheumatic heart disease, congenital heart disease,
pericarditis, and cardiomyopathy may also lead to atrial flutter. Rarely, mitral valve prolapse
or acute myocardial infarction (MI) has been associated with atrial flutter.
In addition, the following conditions are also associated with atrial flutter:
Hypoxia
Pulmonary embolism
Hyperthyroidism
Pheochromocytoma
Diabetes
Electrolyte imbalance
Alcohol consumption
Obesity
Digitalis toxicity
Atrial flutter may be a sequela of open heart surgery. After cardiac surgery, atrial flutter may
be reentrant as a result of natural barriers, atrial incisions, and scar. Some patients develop
atypical left atrial flutter after pulmonary vein isolation for atrial fibrillation.
Although there are no clearly defined genetic conditions that cause atrial flutter, in many
cases there is likely an underlying genetic susceptibility to acquiring it. Genome-wide
association studies (GWAS) have identified genes associated with atrial flutter.[2]
The PITX2 (paired-like homeodomain 2) gene on chromosome locus 4q25 is known to play a
major role in left-right asymmetry of the heart and has been found to have a strong
association with atrial fibrillation[3] and an even stronger association with typical atrial flutter.
[4]
There are not yet any clinically available genetic tests that can identify persons at increased
risk for atrial flutter.
pidemiology
United States statistics
Atrial flutter is much less common than atrial fibrillation. Of the patients admitted to US
hospitals with a diagnosis of supraventricular tachycardia between 1985 and 1990, 77% had
atrial fibrillation and 10% had atrial flutter. On the basis of a study of patients referred to
tertiary care centers, the incidence of atrial flutter in the United States is estimated to be
approximately 200,000 new cases per year.[5]
Sex- and age-related demographics
In a study of 100 patients with atrial flutter, 75% were men. In another study performed at a
tertiary care study, atrial flutter was 2.5 times more common in men.
Patients with atrial flutter, as with atrial fibrillation, tend to be older adults. In one study, the
average age was 64 years. The prevalence of atrial fibrillation increases with age, as follows:
Prognosis
The prognosis for atrial flutter depends on the patients underlying medical condition. Any
prolonged atrial arrhythmia can cause a tachycardia-induced cardiomyopathy. Intervening to
control the ventricular response rate or to return the patient to sinus rhythm is important.
Thrombus formation in the left atrium has been described in patients with atrial flutter (021%). Thromboembolic complications have also been described.[6]
Because of the conduction properties of the AV node, many people with atrial flutter will
have a faster ventricular response than those with atrial fibrillation. The heart rate is often
more difficult to control with atrial flutter than with atrial fibrillation, because of increased
concealed conduction in those with atrial fibrillation.
For the most part, morbidity and mortality result from complications of rate (eg, syncope and
congestive heart failure [CHF]). In patients with atrial flutter, the risk of embolic occurrences
approaches that seen in atrial fibrillation. Patients with Wolff-Parkinson-White syndrome
who develop atrial flutter can develop life-threatening ventricular responses and therefore
should be considered for catheter ablation of their accessory bypass tract.
Data from the Framingham study suggest that patients with atrial fibrillation do not live as
long as patients without atrial fibrillation (ie, control subjects). No data are available on atrial
flutter.
The prognosis for patients with type I atrial flutter who undergo catheter ablation is excellent,
with a very low recurrence rate. The picture is not as clear for patients with both atrial flutter
and atrial fibrillation. Some reports have documented fewer episodes of atrial fibrillation after
successful flutter ablation; others have not. It is possible that atrial fibrillation may be more
responsive to antiarrhythmic agents after atrial flutter has been eliminated.
Bohnen et al performed a prospective study to assess the incidence and predictors of major
complications from contemporary catheter ablation procedures.[7] Major complication rates
ranged from 0.8% (supraventricular tachycardia) to 6% (ventricular tachycardia associated
with structural heart disease), depending on the ablation procedure performed. Renal
insufficiency was the only independent predictor of a major complication.
Numerous reports indicate that patients with atrial fibrillation who are given class IC
antiarrhythmic agents may convert to atrial flutter with faster ventricular rates. Thus, patients
receiving type IC agents (eg, flecainide) should also receive an AV nodeblocking drug such
as a beta blocker or calcium channel blocker. In patients with both atrial fibrillation and atrial
flutter, the relative risk for development of stroke is 4.1% in comparison with control
subjects.[8]
Patient Education
Patient education regarding medications and diet is important. Patients taking warfarin should
avoid making major changes in their diet until they have consulted with their healthcare
providers. Specifically, a sudden change in the consumption of green leafy vegetables, which
are sources of vitamin K, can affect coagulation in patients taking warfarin, which inhibits
vitamin K synthesis. This education is not needed with newer drugs that avoid these drugdrug or drug-food interactions.
For patient education information, see the Heart Health Center, as well as Atrial Flutter,
Heart Rhythm Disorders, Stroke, Supraventricular Tachycardia, and Palpitations.
http://emedicine.medscape.com/article/151210-overview
Updated: Mar 27, 2014